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. 2025 Aug 12;9(15):3900-3904.
doi: 10.1182/bloodadvances.2025016002.

Molecular profiling of primary renal diffuse large B-cell lymphoma unravels a proclivity for immune-privileged tropism

Axel Künstner  1   2 , Vera von Kopylow  1   3   4 , Philipp Lohneis  4 , Matthias Kümmel  1   3   4 , Hanno M Witte  1   3   5 , Lorenz Bastian  1   6 , Veronica Bernard  4 , Stephanie Stölting  4 , Kathrin Kusch  4 , Nikolas von Bubnoff  1   3 , Konrad Steinestel  7 , Annette Arndt  7 , Hartmut Merz  4 , Hauke Busch  1   2 , Alfred C Feller  4 , Niklas Gebauer  1   3
Affiliations

Molecular profiling of primary renal diffuse large B-cell lymphoma unravels a proclivity for immune-privileged tropism

Axel Künstner et al. Blood Adv. .
No abstract available

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Conflict of interest statement

Conflict-of-interest disclosure: N.G. received travel support from BeiGene, Janssen, and Roche, and honoraria from BeiGene, Roche, Takeda, Janssen, Menarini Stemline, and AstraZeneca. The remaining authors declare no competing financial interests.

Figures

Figure 1.
Figure 1.
Molecular landscape of prDLBCL. (A) Venn diagram depicting the number of samples for which whole-exome sequencing (WES; n = 26), RNA-seq (n = 29), and OncoScan (n = 29) were successfully performed. (B) Fusions identified by RNA-seq in prDLBCL samples (beyond MYC/BCL2/BCL6 rearrangements identified in cases studied by fluorescence in situ hybridization [FISH]) displayed by their genomic location. (C) Sankey plot illustrating the distribution of cases of prDLBCL into GCB/non-GCB categories by IHC according to the algorithm proposed by Hans et al as well as by COO classified according to gene expression profiling derived from RNA-seq and lastly according to molecular clusters drawn from the LymphGen algorithm, integrating data from WES, RNA-seq, OncoScan, and FISH (BCL2/BCL6/MYC), depicting the significant degree of molecular heterogeneity. (D) Oncoplot displaying putative driver genes and the number of samples harboring mutations in a given gene (right). Mutation types are color coded, and covariates, including sex, COO, FISH results for BCL2/BCL6/MYC, and type of biopsy (punch/needle core vs open resection/nephrectomy), are shown below for each sample. COO, cell of origin; EBV, Epstein-Barr-Virus; f, female; IHC, immunohistochemistry; m, male; NA, not available.
Figure 2.
Figure 2.
Somatic copy number aberrations in prDLBCL compared with other subtypes of DLBCL including IP-LBCL. (A) Genome-wide frequency of somatic copy number amplifications (red) and deletions (blue) across all chromosomes in prDLBCL. Key regions with recurrent alterations are annotated, including PRDM1, CDKN2A, HLA-B, and NFKBIZ, highlighting their potential involvement in lymphomagenesis and immune evasion. The x-axis represents chromosomal locations, whereas the y-axis indicates the frequency of alterations across the cohort. (B) Amplifications and deletions at recurrently affected loci in an all-comer cohort of DLBCL (first column), DLBCL of ABC and GCB subtypes (second and third column), and IP-LBCL with primary CNS or primary testicular manifestation (columns 4 and 5) compared to prDLBCL (column 6). (C) Impairment of the MHC class I and II apparatus as well as its immediate interaction partners by mutations and/or SCNAs. PTLBL, primary testicular large B-cell lymphoma; SCNA, somatic copy number aberration.
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